Factors responsible for the stimulation of the adrenal medulla during asphyxia in the foetal lamb

Abstract

Previous investigations on the release of catecholamines from the adrenal medulla of the foetal lamb during asphyxia showed that certain characteristic changes occurred during the development of the foetus (Comline & Silver, 1961). From relatively early in pregnancy, 80-90 days (full term 147 days), the adrenal medulla appeared to react directly to asphyxia with a secretion which contained a high proportion of noradrenaline. This response remained unaffected by section of the splanchnic nerves, destruction of the spinal cord, or by hexamethonium and it appeared to be due to the direct effect of asphyxia on the medullary cells. About 15-20 days before the end of gestation a nervous component was demonstrable, which was dependent upon the integrity of the splanchnic nerves, and the secretion then contained large amounts of both adrenaline and noradrenaline. The mechanism for this response, which at the end of pregnancy superseded the direct effect, appeared to lie in the spinal cord, since section at C 1 made little difference to the secretion.In all these experiments (Comline & Silver, 1961) asphyxia was induced by ligation of the umbilical cord, and at that time it was not practicable either to identify the exact nature of the stimuli responsible for the two types of discharge from the adrenal gland, or to determine whether a relation existed between the level of secretion and the severity of asphyxia in these foetuses. The present investigations have been concerned largely with these problems. The changes of Po2, PC02, pH, lactic acid and glucose in the foetal blood during asphyxia which accompany the discharge from the gland have been examined in lambs at different stages of gestation, and the possible factors involved in the response studied under more carefully controlled conditions. It was soon apparent that the output of catecholamines from the adrenal medulla was primarily affected by a fall in foetal arterial Po2; changes in arterial PC02, pH and lactic acid had little effect. Accurate and rapid measurement of both foetal and maternal

Catecholamines in arterial and venous umbilical blood: placental extraction, correlation with fetal hypoxia, and transcutaneous partial oxygen tension

“…Animal experiments have shown that the tcpO 2 varies from the arterial pO 2 after recurrent hypoxic episodes. It appears that vasoconstriction of cutaneous vessels due to increased release of NE during hypoxia may be responsible for the observed tc-art pO 2 -d [6,7,16,17]. The heating element of the electrode obviously is not always capable of maintaining optimal cutaneous blood flow.…”

“…Investigations performed in animal experiments [6,7,16,17,19] as well as in man [2,3,9,10,18,20,25] suggest that fetal hypoxia is associated with an increase in circulating catecholamines due to sympathoadrenal stimulation. The correlation between catecholamines and cardiovascular, respiratory, and metabolic changes as determined during intrapartum fetal monitoring by means of cardiotocography (CTG), fetal blood gas analysis, and measurement of the transcutaneous partial oxygen tension (tcpC^) has not yet been exhaustively investigated.…”

Sympathetic control of the cardiovascular response to acute hypoxemia in the chick embryo

“…In fetal sheep (4,5,27) and neonatal rats (29), at least two mechanisms mediating catecholamine release in response to hypoxemia have been described. First, before functional innervation of the adrenal glands, hypoxemia may stimulate chromaffin cells directly to promote catecholamine release into the circulation.…”

The uterine and maternal placental blood flow during hyperoxia

“…There is, however, a curvilinear relationship, so that the increment of fetal P Oa values for any given change of maternal P Oa will be less the higher the maternal P Oa . This type of relationship has been demonstrated in humans by RORKE et al [10], and in sheep by COMLINE et al [4]. Thus, the fetus appears to be protected from high levels of P O(l [2].…”

“…RORKE et al [10] in humans and several investigators using animals [5,4,1] have demonstrated that an increase of maternal oxygen tension causes only a disproportionately small increase of fetal oxygen tension. Such an effect might be explained by the fact that the placental venous P Oz increases only moderately and thus that the pressure head for oxygen diffusion is not elevated in proportion to maternal arterial P O2 .…”